Does delayed gastric emptying contribute to gastroesophageal reflux disease?

Does Delayed Gastric Emptying Contribute to Gastroesophageal Reflux Disease? Werner Schwizer,

MD,

Ronald A. Hinder,

MD, PhD,

We studied 76 patients with symptoms of heartburn, regurgitation, or both and 38 asymptomatic control subjects by measuring the gastric emptying of technetium-99m-labeled oatmeal. In addition, we performed 24-hour esophageal pH monitoring and manometric studies of the esophagus on all study participants. Endoscopy was performed on all patients. Patients with proved reflux on 24-hour pH monitoring, in comparison to those without reflex and the control subjects, had a shorter lower esophageal segment with a lower pressure and more esophagitis. Delayed gastric emptying occurred with equal frequency in patients with and without reflux. Esophageal reflux was not associated with delayed gastric emptying. Delayed emptying was associated with less esophagitis than found in those with normal gastric emptying, suggesting that the prolonged presence of food in the stomach may have a buffering effect on gastric acidity. We concluded that delayed emptying is not a major factor iu the pathophysiology of gastroesophageal reflux disease and that therapy aimed at speeding gastric emptying cannot be supported by our results.

Tom R. DeMeester,

into the cardia and fundus of the stomach, it is possible that weakening of the sphincter muscle may also cause impairment in gastric motor activity and subsequent delayed gastric emptying [5]. Furthermore, since gastroesophageal reflux is more pronounced in the postprandial phase, prolonged gastric emptying would increase the time at risk for gastroesophageal reflux [6j. Some previous studies have shown no abnormality of gastric emptying in patients with gastroesophageal reflux [7]. Others have indicated that there is delayed gastric emptying of either liquids or solids in less than 50 percent of patients with esophageal reflux disease [8-101. To establish a convincing etiologic relationship between esophageal reflux disease and delayed gastric emptying, it is necessary to analyze the gastric emptying profile in patients with proved gastroesophageal reflux. It is also necessary to determine whether poor sphincter function along with delayed gastric emptying results in excessive gastroesophageal reflux, if delayed gastric emptying explains the cause of reflux through a sphincter with normal function, and whether delayed gastric emptying contributes to the development of esophagitis. Therefore, we studied 76 symptomatic patients with a clinical history suggestive of gastroesophageal reflux and, by creating various subpopulations, correlated 24-hour esophageal pH recordings, esophageal manometry, and endoscopic findings with the rate of gastric emptying in an effort to define an etiologic relationship between gastric emptying and gastroesophageal reflux. MATERIAL

I

t seems logical that in patients with gastroesophageal reflux disease, in whom esophageal mucosal damage is caused by secretions that have refluxed from the stomach, an etiologic mechanism might involve the abnormal accumulation of food and secretions in the stomach with reflux of this material past an incompetent lower esophageal sphincter. This would occur in patients with poor gastric emptying and would be aided by the fact that the associated dilatation of the stomach could conceivably cause shortening of the lower esophageal sphincter with consequent sphincter incompetence [I ,2]. Gastroesophageal reflux disease has indeed been linked convincingly with impaired lower esophageal sphincter function [I ,3,4]. Conversely, since both circular and longitudinal muscle fibers of the lower esophageal sphincter continue From the Department of Surgery, Creighton University, Omaha, Nebraska. Requests for reprints should be addressed to Ronald A. Hinder, MD, Department of Surgery, Creighton University, 601 North 30th Street, Omaha, Nebraska 68 13 1. Presented at the 29th Annual Meeting of the Society for Surgery of the Alimentary Tract, New Orleans, Louisiana, May 17-18, 1988.

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MD, Omaha, Nebraska

AND METHODS

The control group consisted of 38 volunteers who on interview did not have a history of foregut symptoms, upper gastrointestinal disease, or previous gastrointestinal surgery. All had normal findings on upper gastrointestinal roentgenographic barium study, esophageal manometry, 24-hour esophageal pH monitoring, and gastric emptying scans. The demographic data are shown in Table I. Informed consent was obtained, and the study was approved by the Creighton University Human Research Committee. The patient population consisted of 76 consecutive patients referred between 1984 and 1987 to the Creighton University Gastrointestinal Diagnostic and Research Center with symptoms typical of gastroesophageal reflux disease (heartburn, regurgitation, dysphagia, chest pain, epigastric pain, or chronic cough). For entry into the trial, patients were required to have at least chronic heartburn or regurgitation. Patients with achalasia, scleroderma, or previous gastric or esophageal surgery were excluded. Esophageal manometry, 24-hour esophageal pH monitoring, endoscopy, and gastric emptying scanning were performed on all patients. The demographic data are shown in Table I. 157

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1989

TABLE I Demographks, Manometry, and Ro8ultr of 2Gttour

Control&oup(n = 38) Median Range

MeMfsD

Age (~0 Sex(1:m) HeIf@ Weight (kg) Manometry Pressure(mmHg) OL(cm) AL(cm)

pH MemIterIngIn Controls Subjects and Patient8

36.1 f 11.1 23:15 172 f 9 73.6 f 16.7

34

14.2 f 5.1 3.7 l 0.7 2.2 * 0.7

24-howpHmcdtorlng Totaltime< pli4(%) While UprIght While suplns Totaleplscdes 5 mln (n) Longestepisode(mln)

1.4 f 2.5 f 0.7 f 25.4 f 1f 6.5 l

AL = abdomlnalIength;OL

- overall length.

2.5 2.8 1.1 24.7 1.3 7

PatlentGroup(n= 76) Madlan Renge

MMtlfSD

172 70.6

23-71 . 157-166 50-132

49.7 i 15.3 34:42 169.9l 11 84.2 f 16.9

170 63.3

13 3.6 2.2

5-27 2.4-5.5 0.8-5

9.5 f 5.6 2.9 f 1.1 1.3 l 0.8

1.1 1.7 0.1 21 0 4

O-6 O-10 o-4 O-126 o-5 o-29

10.2l 10.4f 9.2 f aa.af 6.7 k 21.9 f

52.5

16-60 150-193 46.5-121.5

3 1.2

O-30 o-6.8 o-3.7